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Preparation Questions-Critical Care Simulation #1

1. What is Acute Coronary Syndrome (ACS)?


Acute coronary Syndrome is prolonged ischemia of the heart, it is a
spectrum of unstable angina, non ST segment (NSTEMI), and ST
elevation (STEMI)
2. Describe the etiology and pathophysiology of ACS.
Atherosclerosis of coronary arteries forms plaques that rupture and
initiate inflammation and cause platelets to aggregate to the area and
form a thrombus. The thrombus blocks blood flow through coronary
arteries causing ischemia of myocardial cells. The thrombus can cause
partial occlusion (unstable angina, or an NSTEMI), or complete
occlusion (STEMI)
3. What are the differences between a transmural (e.g., full thickness)
myocardial infarction (MI) and a subendocardial (e.g., partial thickness)
MI?
Full thickness necrosis takes 4-6 hour of ischemia to develop, and
involves at 3 layers of the heart muscle, STEMI
Partial thickness involves one area of the heart, NSTEMI
4. How are these differences depicted on the ECG?
STEMI
o ST elevation, ischemia long enough to cause permanent damage
NSTEMI
o ST depression and/or inverted T waves, injury is reversible if get
blood flow back quickly
Pathological Q wave- abnormal or absent depolarization in damaged
tissue, infarct, associated with STEMI
5. What are the areas of infarction?
Anterior, inferior, lateral, septal, or posterior wall
6. How does the location and area of the artery correlate with the part of
the coronary circulation:
Right coronary artery- inferior wall
Left anterior descending artery- anterior wall
Left circumflex artery- lateral and or posterior wall
7. Why does the younger person who has a severe MI usually have more
serious impairment than an older person?
The severity of an MI depends on preexisting collateral circulation;
elderly people with CAD and atherosclerosis that develop over time
develop collateral circulation that can supply the area around the

blockage with blood. In a younger person they don't have that


adaptation developed to help the heart deal with the ischemia.
8. Why is it common for the temperature to rise in the first 24 hours
following an AMI?
The elevation in temperature is from the bodys activation of the
inflammatory process and increase in white blood cells. Dead cardiac
cells release enzymes that stimulate breakdown of the dead tissue and
are markers that an MI has occurred. Collateral circulation develops to
improve blood flow to affected areas and increased levels of plasma
glucose can be used for anaerobic metabolism (why blood glucose is
measured after an MI)
9. What is the most common complication following an AMI? Why?
Dysrhythmias are the most common complication after and MI. A
myocardial infarction affects myocardial cells sensitivity to impulses
and can cause a dysrhythmia.
Life threatening dysrhythmias occur mostly with anterior wall
infarction, Heart blocks happen when an important part of the
conduction system is destroyed, and ventricular fibrillation is a lethal
dysrhythmia and most often happen 4 hours after pain starts.
10.
What are the side effects/complication commonly seen in the
following areas of infarction:
Inferior wall damage
Lateral wall damage
Anterior wall damage
Posterior wall damage
11.
What are the serum cardiac markers used for diagnosing an AMI?
When do their levels peak? When do their levels return to normal?
Cardiac specific troponin: cardiac specific troponin T (cTnT) and cardiac
specific troponin 1 (cTn1)- levels increase 4-6 hours after an MI and
peak at 10-24 hours and lower to baseline in 10-14 days
Creatine kinase (CK)- rise 6 hours after peak at 18 and go back to
normal 24-36 hours
o MB (CK-MB)- specific to myocardial cells and quantify
mycocardial damage
Myoglobin is released 2 hours after an MI, peaks 13-15 hours, is it not
myocardial specific
12.
Within how many hours of the onset of pain should thrombolytic
therapy be instituted to be most beneficial to the patient? What are the

nursing implications and management of the patient receiving


thrombolytic therapy?
Thrombolytic therapy should be given as soon as possible within the
first hour and before 6 hours after symptoms begin.
Draw blood to get baseline lab values and start multiple IVs. Monitor
heart rhythm, vital signs, pulse ox and assess heart and lung sounds.
Observe from bleeding because other clots are broken up as well as
the coronary arteries. Assess neurologic status for cerebral bleed.
Observe ECG for changes.

13.
What are the major drug classifications the nurse would
anticipate a patient with ACS receiving? For each of the classifications,
identify the action and key nursing implications.
IV nitroglycerin- reduces angina pain and help blood flow, decreased
preload and afterload and increases myocardial oxygen supply.
Monitor BP for hypotension, IV fluid bolus. To help tolerance titrate
dose down at night and up during the day.
Morphine Sulfate- help chest pain, vasodilator, lowers myocardial
oxygen consumption, reduce anxiety. Monitor respirations because
of respiratory depression, hypotension.
Beta adrenergic blockers- reduce heart rate, BP and contractility,
reduces the risk of reoccurrence of MI.
ACE inhibitors- start within first 24 hours especially if STEMI or
anterior wall damage. Help prevent ventricular remodeling and
prevent/slow heart failure. If can not tolerate start angiotension 2
receptor blockers
Antidysrhythmic drugs- prevent the most common complication
from an MI.
Lipid lowering drugs- lipid panel done and given to patients with
elevated triglycerides and LDL
Stool softeners- constipated from bed rest and opioids. Prevent
straining and vagal stimulation from valsalva maneuver that can
cause bradycardia and lead to a dysrhythmia.
14.
What is the half-life of amiodarone? Why is this important for the
learners to know?
Amiodarone has a long half-life of about 58 days and is stored in fat
tissues and organs and cause cause adverse side effects involving
the lungs, liver, thyroid and other organs.

Reference List

Lewis, S., Dirksen, S., Heitkemper, M., Bucher, L., & Camera, I. (2011).
Medical-surgical
nursing: Assessment and management of clinical problems (8th ed.). St.
Louis: Mosby
Elsevier.